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目的:观察抗血小板溶栓素(anti-platelet thrombolysin,APT)对缺血性脑损伤的保护作用并初步探讨其作用机制。方法:SD大鼠,随机分为假手术组(Sham)、模型组(缺血再灌注组)、阳性组(依达拉奉注射液)、APT高、中、低组。双侧颈动脉结扎,建立脑缺血模型,测定大鼠脑含水量,HE染色观察脑组织病理改变;线栓法建立大鼠脑缺血/再灌注模型,进行行为学评分,酶联免疫法(ELISA)及免疫组化测定脑组织中Toll样受体4(TLR4)、c-Jun氨基末端激酶(JNK)、Bax蛋白含量。结果:与模型组比较,APT高、中剂量组可明显改善缺血再灌注后大鼠神经功能障碍症状,降低脑水肿程度,改善缺血后脑组织的病理改变,明显降低缺血后脑组织中TLR4、JNK、Bax蛋白表达。结论:APT对缺血性脑损伤有较好的保护作用,其机制可能与抑制脑组织中TLR4/JNK/Bax信号通路表达,从而抑制细胞凋亡有关。
Objective: To observe the protective effect of anti-platelet thrombolysin (APT) on ischemic brain injury and to explore its mechanism. Methods: SD rats were randomly divided into sham group, model group (ischemic reperfusion group), positive group (edaravone injection), APT high, medium and low groups. The bilateral carotid artery was ligated, the model of cerebral ischemia was established, the water content of rat brain was measured, the pathological changes of brain tissue were observed by HE staining, the model of cerebral ischemia / reperfusion was established by thread occlusion, and the behavior score and enzyme-linked immunosorbent assay The levels of Toll-like receptor 4 (TLR4), c-Jun N-terminal kinase (JNK) and Bax were measured by ELISA and immunohistochemistry. Results: Compared with the model group, high and medium doses of APT could significantly improve the symptoms of neurological dysfunction, reduce the degree of cerebral edema, improve the pathological changes of ischemic brain tissue, and significantly reduce the expression of TLR4 , JNK, Bax protein expression. CONCLUSION: APT has a good protective effect on ischemic brain injury. The mechanism may be related to the inhibition of TLR4 / JNK / Bax signaling pathway and the inhibition of apoptosis in brain tissue.